The major objective of our research is to understand how damage to DNA by chemical carcinogens is repaired by normal cultured human diploid fibroblasts and fibroblasts from individuals with increased risk of cancer and defects in DNA repair (seroderma pigmentosum, xeroderma pigmentosum variants, Fanconi's anemia and ataxia telangiectasia). In the coming year we plan to continue our work on the intragenomal distribution of damage and repair (both removal of damage and DNA repair synthesis). Efforts are underway to develop subcellular systems for analyzing the repair process.